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Your search keyword '"B, Malitschek"' showing total 2 results
Start Over Author "B, Malitschek" Journal annals of neurology
2 results on '"B, Malitschek"'

1. Up-regulation of the metabotropic glutamate receptor mGluR4 in hippocampal neurons with reduced seizure vulnerability

Author

A A, Lie, A, Becker, K, Behle, H, Beck, B, Malitschek, P J, Conn, R, Kuhn, R, Nitsch, M, Plaschke, J, Schramm, C E, Elger, O D, Wiestler, and I, Blümcke

Subjects
Adult, Male, Neurons, Epilepsy, Complex Partial, Humans, Female, Microscopy, Immunoelectron, Receptors, Metabotropic Glutamate, Hippocampus, Immunohistochemistry, In Situ Hybridization, Up-Regulation
Abstract

Selective hippocampal cell loss and altered neurotransmitter receptor expression have been proposed as pathogenic mechanisms in the development of chronic mesial temporal lobe epilepsy (TLE). Studies in animal models point to metabotropic glutamate receptors (mGluRs) as modulators of hippocampal epileptogenesis. In addition, mGluRs may constitute specific targets for the development of novel anticonvulsive drugs. As mGluR4 represents an inhibitory class III mGluR associated with the reduction of intracellular cyclic AMP levels and calcium influx, we have analyzed the regional and cellular expression of mGluR4 in surgical hippocampal specimens obtained from patients with TLE by using immunohistochemistry and in situ hybridization. Although the hippocampi of control specimens (n = 11) were almost devoid of mGluR4 immunolabeling, all TLE specimens (n = 35) showed a striking up-regulation of mGluR4 immunoreactivity, in particular within the dentate gyrus. Immunoelectron microscopy localized the receptor protein to the periphery of presynaptic and postsynaptic membranes. In situ hybridization revealed increased transcript levels of mGluR4 in dentate granule cells and residual CA4 neurons of TLE specimens compared with controls. Our results suggest a potential role of mGluR4 in counteracting excitatory hippocampal activity and in modulating seizure-associated vulnerability of hippocampal neurons. These data may also provide a basis for pharmacological studies of mGluR4 agonists as potential novel drugs in the treatment of TLE.

Published
2000

2. Up-regulation of the metabotropic glutamate receptor mGluR4 in hippocampal neurons with reduced seizure vulnerability.

Author

Lie AA, Becker A, Behle K, Beck H, Malitschek B, Conn PJ, Kuhn R, Nitsch R, Plaschke M, Schramm J, Elger CE, Wiestler OD, and Blümcke I

Subjects
Adult, Epilepsy, Complex Partial pathology, Female, Hippocampus pathology, Hippocampus ultrastructure, Humans, Immunohistochemistry, In Situ Hybridization, Male, Microscopy, Immunoelectron, Neurons physiology, Neurons ultrastructure, Receptors, Metabotropic Glutamate physiology, Epilepsy, Complex Partial physiopathology, Hippocampus physiopathology, Neurons pathology, Receptors, Metabotropic Glutamate analysis, Up-Regulation
Abstract

Selective hippocampal cell loss and altered neurotransmitter receptor expression have been proposed as pathogenic mechanisms in the development of chronic mesial temporal lobe epilepsy (TLE). Studies in animal models point to metabotropic glutamate receptors (mGluRs) as modulators of hippocampal epileptogenesis. In addition, mGluRs may constitute specific targets for the development of novel anticonvulsive drugs. As mGluR4 represents an inhibitory class III mGluR associated with the reduction of intracellular cyclic AMP levels and calcium influx, we have analyzed the regional and cellular expression of mGluR4 in surgical hippocampal specimens obtained from patients with TLE by using immunohistochemistry and in situ hybridization. Although the hippocampi of control specimens (n = 11) were almost devoid of mGluR4 immunolabeling, all TLE specimens (n = 35) showed a striking up-regulation of mGluR4 immunoreactivity, in particular within the dentate gyrus. Immunoelectron microscopy localized the receptor protein to the periphery of presynaptic and postsynaptic membranes. In situ hybridization revealed increased transcript levels of mGluR4 in dentate granule cells and residual CA4 neurons of TLE specimens compared with controls. Our results suggest a potential role of mGluR4 in counteracting excitatory hippocampal activity and in modulating seizure-associated vulnerability of hippocampal neurons. These data may also provide a basis for pharmacological studies of mGluR4 agonists as potential novel drugs in the treatment of TLE.

Published
2000

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